Abstract
ABSTRACT
【Background/Aim】Functional decline in the abdominal and external anal sphincter (EAS) muscles due to diabetic neuropathy (DN) can impair evacuation and continence mechanisms. However, the relationship between this decline and fecal excretion function remains unclear. This study investigates the effects of diabetes on the abdominal and EAS muscles, which are controlled by somatic nerves.
【Method】Type 1 diabetes was induced in 18 animals using streptozotocin (STZ), while 20 age-matched control animals were injected with a saline solution. We recorded rectal pressure and fatigability during stimulation of the nerves innervating the abdominal muscles, as well as the closing pressure and fatigability of the EAS muscle during nerve stimulation. Changes in each muscle type were analyzed.
【Results】The diabetic group exhibited lower rectal pressure output during abdominal muscle stimulation compared to the control group. Additionally, the diabetic group showed a slower decline in fatigability. No significant difference in anal closing pressure was observed between the diabetic and control groups during EAS muscle stimulation, nor were there significant differences in fatigability. In abdominal muscle fibers, the diabetic group experienced a decrease in type 2B fibers and an increase in type 2X fibers. No differences were observed in the EAS muscle between the diabetic and control groups.
【Discussion】Diabetes more significantly affects muscle strength in the abdominal muscles than in the EAS muscle, potentially causing an imbalance between reduced abdominal pressure, which aids defecation, and anal closure pressure, which aids in stool storage. This study reveals that in diabetic conditions, somatically innervated EAS muscles experience a slower decline compared to abdominal and limb muscles.
